Learn / FMK
Every FMK condition
299 diseases, deficiencies, toxicities and drug mechanisms harvested from every FMK deck — the ones sprinkled through a single bullet as much as the ones with their own slide. Pick what you're given and what you have to name, or let it cycle; distractors come from the same category so you have to discriminate (hypoketotic vs. ketotic hypoglycemia, which GSD, which urea-cycle enzyme…). Every answer shows the whole card with the lecture and slide.
Toxin/Drug · FMK 01.5
Ethylene glycol (antifreeze) poisoning Acquired / not inherited
Defect / target: Alcohol dehydrogenase converts ethylene glycol to toxic metabolites (glycolate, oxalate)
Mechanism: Ethylene glycol is a substrate of alcohol dehydrogenase and is oxidized to toxic acids that cause metabolic acidosis and calcium oxalate renal injury.
↑ Accumulates: Glycolic acid, oxalate (calcium oxalate crystals)
Presentation: Inebriation, anion-gap metabolic acidosis, acute kidney injury
Labs: Anion-gap acidosis, osmolar gap, calcium oxalate crystals in urine
Treatment: Ethanol (100-fold higher ADH affinity, competitive inhibitor) or fomepizole
Ethanol out-competes ethylene glycol for the ADH active site: competitive inhibition raises Km, Vmax unchanged
Learn the mechanism: Ethanol metabolism →
FMK 01.5 Enzyme Kinetics, Regulation and Inhibition · slide 2, 13